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Polycystic kidney disease ( PKD ) and other renal ciliopathies are characterized by cysts, inflammation, and fibrosis. Cilia function as signaling centers, but a molecular link to inflammation in the kidney has not been established. Here, we show that cilia in renal epithelia activate chemokine signaling to recruit inflammatory cells. We identify a complex of the ciliary kinase  LKB 1 and several ciliopathy‐related proteins including  NPHP 1 and  PKD 1. At homeostasis, this ciliary module suppresses expression of the chemokine  CCL 2 in tubular epithelial cells. Deletion of  LKB 1 or  PKD 1 in mouse renal tubules elevates  CCL 2 expression in a cell‐autonomous manner and results in peritubular accumulation of  CCR 2 +  mononuclear phagocytes, promoting a ciliopathy phenotype. Our findings establish an epithelial organelle, the cilium, as a gatekeeper of tissue immune cell numbers. This represents an unexpected disease mechanism for renal ciliopathies and establishes a new model for how epithelial cells regulate immune cells to affect tissue homeostasis.

Cilia‐localized LKB 1 regulates chemokine signaling, macrophage recruitment, and tissue homeostasis in the kidney